DNA repair in mitotically growing cells of the yeast Saccharomyces cerevisiae is under the control of more than 20 genetic loci. The products of some genes have been shown to be involved in normal meiosis. We have developed sucrose gradient techniques for the examination of repair events in mitotically growing cells and meiotically developing cells after low doses of UV and ionizing radiation to wild type and repair-defective strains. Using these techniques we are determining the role of mitotically identified repair functions on damage occurring during meiosis. We have demonstrated that wild type cells efficiently excise UV-induced pyrimidine dimers both as mitotically growing or meiotic cells. Excision is blocked in a rad1 throughout meiosis suggesting that there are no additional excision repair systems during meiosis. As found for mitotic growth, DNA synthesis proceeds past UV-induced pyrimidine dimers during meiosis indicating that there is a general ability to bypass lesions in the DNA. The bypass mechanism does not appear to involve recombination. In fact, the presence of damage appears to inhibit the meiotic round of genetic recombination whereas it stimulates recombination in mitotically growing cells.